Lipase, pancreatic amylase, and total amylase activities were measured in nondiseased and diseased human pancreatic tissues and in six different locations of the human digestive system. In addition, it was determined whether serum lipase and pancreatic amylase tests could replace the total amylase test to improved diagnostic efficiency in the evaluation of acute pancreatitis in hyperamylasemia patients. Nondiseased pancreatic tissue contained 4.5 times more lipase activity than total amylase activity. Diseased pancreatic tissue contained less activity for both lipase and total amylase compared to normal tissue. The total amylase activity of the pancreas was comprised solely of pancreatic amylase. Tissue obtained from six different anatomic locations in the digestive system contained 35 to 45 times less lipase and total amylase activity compared to the pancreas. Total amylase activity of the digestive system tissues were comprised of 25% pancreatic and 75% salivary isoamylases. Lipase, pancreatic amylase, and total amylase levels also were determined in serial serum samples from 17 consecutive hyperamylasemia patients admitted with possible acute pancreatitis. The serum lipase level remained higher than normal longer than either the total amylase and pancreatic amylase levels. In patients with hyperamylasemia of pancreatic origin, a poor correlation was observed at admission between serum pancreatic amylase and serum lipase. Not all patients with elevated lipase had an elevated pancreatic amylase level and vice versa. However, in every patient pancreatic disease would have been detected by the elevation of either lipase or pancreatic amylase levels. Diagnostic efficiency for pancreatic disease using serum pancreatic amylase, lipase, and total amylase tests was 94.1%, 76.5%, and 64.7%, respectively. These data suggest that lipase and pancreatic amylase tests are specific for the pancreas and might be considered replacements for total amylase as the stat or routine laboratory test for the diagnosis of pancreatic tissue injury.
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http://dx.doi.org/10.1093/ajcp/96.5.610 | DOI Listing |
Acute pancreatitis (AP) is a life-threatening condition, with a higher mortality rate in men than women and in which estrogens might play a protective role. This study aimed to investigate sex-dependent differences in a mouse model of caerulein-induced AP. Thirty-six C57BL/6J mice (19 females and 17 males) were treated intraperitoneally with phosphate-buffered saline or caerulein, and sacrificed 12 hours, 2 days, or 7 days after the last injection.
View Article and Find Full Text PDFLangenbecks Arch Surg
January 2025
Hepatopancreatobiliary Center, Beijing Tsinghua Changgung Hospital, School of Clinical Medicine, Tsinghua University, Beijing, China.
Purpose: To investigate the risk factors for late postoperative pancreatic fistula (POPF) following pancreaticoduodenectomy (PD), with a focus on positive drain fluid culture (DFC) results on postoperative day (POD) 1.
Methods: Medical records of 198 patients who underwent PD with drain fluid amylase (DFA) on POD 5 < 3x upper limit of normal (ULN) were included. Late POPF was defined as POPF diagnosed post-POD 6, with DFA on POD 5 < 3xULN.
J Transl Med
January 2025
Hepatology Laboratory, Solid Tumors Program, CIMA, CCUN, University of Navarra, Pamplona, Spain.
Background: Acute pancreatitis (AP) presents a significant clinical challenge with limited therapeutic options. The complex etiology and pathophysiology of AP emphasize the need for innovative treatments. This study explores mRNA-based therapies delivering fibroblast growth factor 21 (FGF21) and apolipoprotein A1 (APOA1), alone and in combination, for treating experimental AP.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
Department of Pediatric Nephrology, Istanbul University- Cerrahpasa, Cerrahpasa Faculty of Medicine, 34098, Istanbul, Turkey.
Autosomal recessive proximal renal tubular acidosis (AR-pRTA) with ocular abnormalities is a rare syndrome caused by variants in the SLC4A4 gene, which encodes Na/HCO3 cotransporter (NBCe1). The syndrome primarily affects the kidneys, but also causes extra-renal manifestations. Pancreatic type NBCe1 is located at the basolateral membrane of the pancreatic ductal cells and together with CFTR chloride channel, it is involved in bicarbonate secretion.
View Article and Find Full Text PDFRespir Med Case Rep
January 2025
Thoracic Medicine and Surgery, Lewis Katz School of Medicine at Temple University, Philadelphia, PA, United States.
Pancreatopleural fistulas, rare complications of chronic pancreatitis, are often overlooked in the initial differential diagnoses of pleural effusions, resulting in delayed diagnosis and management. We present the case of an elderly male with recurrent pleural effusion and a history of chronic pancreatitis. Diagnostic challenges arose, with the initial misdiagnosis as pneumonia.
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